The present disclosure relates to the diagnosis and therapy of sleep disorders.
More particularly, the disclosure relates to a “kinesthetic stimulation” device which is a device for external sensory stimulation of the patient by a vibrator in contact with the skin in a sensitive and precise region of the body of the patient. Activating this vibrator has the effect of locally exciting cutaneous or mechanoreceptor endings of the skin, and triggering a response from the patient's autonomic nervous system, with sympathetic predominance (hereinafter “autonomic response”).
The autonomic response to sympathetic activation is observable on the major modulator effects of cardiac activity, for example a chronotropic effect (e.g., a heart rate increase, a decrease in RR intervals, etc.) and an inotropic effect (e.g., heart contractility increase, etc.). This autonomic response is also observable on the peripheral vasoconstriction, which is increased during sympathetic autonomic activation. In addition to these effects on cardiac activity, a sympathetic activation causes responses in the respiratory system and/or in the central nervous system (autonomic awakenings).
This is a noninvasive method for acting on a number of sleep disorders in alternative ways to the conventional therapeutic approaches that are based on the application of a continuous positive airway pressure through a face mask (a therapy by CPAP), the use of a mandibular orthosis, and/or electrical stimulation of the hypoglossal nerve, which involves the implantation of a pacemaker.
In particular, the respiratory disease known as “sleep apnea syndrome” (SAS) is characterized by the frequent occurrence (at least 10 to 20 times per hour) of apneas during a patient's sleep phase, an “apnea” (or respiratory pause) being defined as a temporary cessation of breathing for a duration longer than 10 s. SAS can also be characterized by the occurrence of hypopnea under the same conditions, a “hypopnea” being defined as a significant decrease (without interruption) of the breathing rate, typically a decrease of more than 50% compared to a previous reference average value.
This pathology reaches more than 4% of the population and more than 50% of patients with heart failure. To protect the individual against asphyxiation due to the decrease in blood oxygen concentration during the interruption or the reduction of respiratory rate, the body adapts itself but with a deleterious effect on sleep, causing unconscious micro-arousals. The consequence is daytime sleepiness when in a wakeful stage, with loss of attention and increased risk of accident. Furthermore, several studies have shown a higher incidence of blood disorders in patients with SAS such as hypertension, ventricular arrhythmias, myocardial infarction and heart failure.
Several documents describe the ability to stop apnea episodes through a stimulation therapy. For example, U.S. Pat. No. 5,555,891 A describes a vibrotactile stimulation system to stop apnea in newborns. The objective is to provide a system capable of detecting apnea and of stimulating the child to stop apnea, with a stimulation energy that may vary to avoid habituation. The applied energy is important and often involves arousal.
WO2007141345 A1 describes a remote monitoring system for neonatal units, to detect and stimulate infant apnea-bradycardia. This application refers to an adjustment of the stimulation energy based on the measured heart rate of the infant. In the proposed method, no analysis of respiratory signals is performed. This prevents the differentiation of types of detected or expected sleep disorders, and therefore, the adjustment of stimulation strategies based on said type of disorder. Moreover, this approach limits the delivery of therapy to the time interval during which the disorder is present.
WO 96/28093 A1 also teaches a system that delivers a stimulus to reduce the frequency or duration of an apnea episode. At the stimulation level, this document simply describes the low and high limits of the stimulation energy that may stop apnea without waking the patient.
US 2008/009915 A1 discloses a system that detects respiratory disorders using a nasal or other cannula and applies a particular vibratory stimulation in the ear region. The objective is to stop apnea, without waking the patient, by stimulation which may be manually or automatically adjusted, depending on physiological characteristics of the patient or of the sleep cycles. This document also generally cites the optimization of the stimulation parameters to fit the severity of the patient's disorder, without giving details on the stimulation parameters adjustment. A change in parameters to prevent habituation is also cited.
US 2010/0048985 A1 describes a similar device for applying stimuli by various natures (e.g., audio or ultrasonic stimulation of the ear, eye stimulation, mechanical stirrer, etc.). The device also analyzes the respiratory activity to evaluate the effectiveness of the stimulation so that the patient or the physician can change the setting of the generator as desired with different doses of the stimuli.
US 2008/0154330 A1 describes an electrical stimulation system of the diaphragm to stabilize breathing. Therapy is triggered when a respiratory instability is detected and stopped when a predetermined number of stable cycles were detected. No indication is given about a possible optimization of the therapy based on a respiration stability analysis. Moreover, this therapy by stimulation of the diaphragm is not applicable to obstructive apnea or hypopnea.
Finally, WO 2009/154458 A2 teaches a system which detects apnea and in turn causes an inspiration reflex by stimulation in the ear region. Various apnea detection methods are illustrated. The stimulation may be electrical or mechanical. The stimulation strategy is minimal; it is to apply pulse trains as long as the disorder is present. However, it is indicated that the stimulation parameters may vary, without, proposed variation rules. A random variation of the parameters is also cited to avoid habituation. However, this document is very vague on the stimulation parameters. It only very generally discloses:
Mechanical, electrical or acoustic stimulation;
A stimulation frequency between 1 and 500 Hz; and
A duration of stimulation and a waiting time between two stimuli varying between 0.5 and 10 s.
The stimulation will be more or less effective depending on the chosen values, for example the brainstem elements have a sensitivity which varies greatly with the frequency range. Furthermore, by randomly varying the stimulation energy, the risk is a less effective therapy (if energy is too low) or waking the patient (if energy is too high). Finally, in this document, the therapy stops as soon as there is respiratory recovery, such as from the detection of an inspiratory reflex that is expected to be triggered.
Thus the prior art provides very little teaching on a precise method for the stimulation delivery. However, a poorly adjusted or random stimulation can cause:
Inefficiency, if the stimulation is not appropriate and adapted to the response that is desired to be caused by the stimulation;
Short or medium term addiction resulting in an ineffective therapy, if the therapy is issued too often or misused;
Finally, a patient arousal and therefore sleep disintegration, which is to be avoided by treating the apnea.